Affordable Access

Access to the full text

Salidroside regulates the expressions of IL-6 and defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways

Authors
  • Wang, Jiawen1
  • Pan, Yibin1
  • Cao, Yongqing1
  • Zhou, Wei1
  • Lu, Jingen1
  • 1 Department of Anal & Intestinal Disease, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200032, P.R.China
Type
Published Article
Journal
Iranian Journal of Basic Medical Sciences
Publisher
Mashhad University of Medical Sciences
Publication Date
Jan 01, 2019
Volume
22
Issue
1
Pages
31–37
Identifiers
DOI: 10.22038/ijbms.2018.26994.6602
PMID: 30944705
PMCID: PMC6437463
Source
PubMed Central
Keywords
License
Green

Abstract

Objective(s): To reveal the detailed mechanism underlying the functions of salidroside on the inflammation of intestinal epithelial cells during IBD. Materials and Methods: Quantitative real-time PCR was employed to assess the expression of IL-6, IL-10, and α-defensins 5 and 6. ELISA assay was performed to measure the secretion of IL-6 and IL-10. MTT assay was used to determine the cell viability and proliferation. Western blot was used to assess the phosphorylation of NF-kB, Erk1/2, JNK, P38, JAK2, and STAT3. Results: Salidroside impaired the proliferation of intestinal epithelial cells at high concentrations ( P < 0.05) and down-regulated interleukin-6 (IL-6) production induced by LPS ( P <0.05). Western blot results showed that salidroside repressed the phosphorylation of NF-kB, Erk1/2, JNK, P38, JAK2 and STAT3 ( P <0.05) and attenuated the activation of NF-κB, MAPK, and STAT3 pathways. Moreover, the expressions of α-defensin 5 and 6 were rescued by salidroside after LPS or SAC triggering ( P <0.05). Conclusion: In summary, salidroside suppressed the expression of IL-6 and elevated the expression of defensins in LPS-activated intestinal epithelial cells through NF-κB/MAPK and STAT3 pathways. The mechanism revealed here may be potentially useful for the treatment of IBD with salidroside.

Report this publication

Statistics

Seen <100 times